Anesthesia in patient with respiratory disease

Anesthesia In Patient with
Respiratory Diseases
Dr. Radhwan H. AL-Khashab
Consultant anaesthesia & ICU
2022

Introduction
 Patients with respiratory diseases account for most common
challenges for the anesthesiologist during daily works.
 Preoperative pulmonary impairment are associated with more
marked intraoperative alterations in respiratory function and
higher rates of postoperative pulmonary complications.

 COPD is currently the 4th leading cause of death in the world
 COPD is projected to be the 3rd leading cause of death by
2020
 More than 3 million people died of COPD in 2012 accounting
for 6% of all deaths globally.

Patients related: Procedures related:
Preoperative risk factors
1. Age > 60 years.
2. ASA > II.
3. Congestive Heart Failure.
4. Preexisting pulmonary dis.
5. Cigarette smoking.
6. Alcohol use.
7. Abnormal results in chest
examination
1) Emergency surgery.
2) Abdominal or thoracic
surgery.
3) Prolonged duration of
anaesthesia > 2.5 hr.
4) Prolonged surgery.
5) Head and neck surgery.
6) Vascular surgery.
7) Use of general anesthesia.
oLaprascopic vs open surgery!

Other risk factors that include:
 Decreased functional status.
 Altered mental status.
 Weight loss greater than 10% within the last 6 months.
 Chronic kidney disease.
 Diabetes mellitus.
 Preoperative anemia (hemoglobin 10 g/dL) .
Elderly patients have increased risk of PPCs even after adjusting
for comorbidities.Advanced age is accompanied by decreased
elastic recoil of lung parenchyma, decreased chest wall
compliance, decreased alveolar surface area, and decreased
respiratory muscle strength

Effct of anesthesia
Several factors contribute to the harmful effects of general
anesthesia on the lungs.
 Instrumentation alters mucociliary function, promoting retention of
secretions.
 Administered drugs release circulating mediators causing
bronchoconstriction.
 There is decreased surfactant production.
 There is inhibition of alveolar macrophage activity.
 NMBA: Their use increases the risk for postoperative desaturation
and postoperative residual curarization (PORC). PORC is an
incomplete recovery from nondepolarizing neuromuscular blocking
agents. Long-acting blockade agents can have residual effects up
to 7 days postoperatively, so better to use medium acting muscle
relaxant.

Ventilator Strategies
 There is strong evidence for the beneficial use of lower tidal
volumes, General surgical patients who undergo intraoperative
mechanical ventilation with lower tidal volumes have lower
levels of circulating inflammatory cytokines postoperatively ,
and may have a lower instance of pneumonia.
 The use of positive end-expiratory pressure (PEEP) is
generally a safe strategy that reduces the incidence and
severity of atelectasis.

Preoperative investigations
There are many investigations used at preoperative time to assess the
tolerability for surgery & anaesthesia.
Routine preoperative laboratory testing may help identify patients at
increased risk.
Other than routine one we may do :
 Pulmonary function test (PFT) , A forced expiratory volume at one second
(FEV1) less than 60% of predicted has been identified as a risk factor for
postoperative complications.
 Blood gases.
 Chest radiographs .
 Preoperative protein depletion is associated with altered pulmonary
dynamics and respiratory muscle function, which leads to a higher rate of
pneumonia , Patients with low serum albumin levels (less than 30 g/L)
have significantly increased rates of reintubation, pneumonia, and failure
to wean from mechanical ventilation

Can we do anything to reduce a
perioperative respiratory complications?
Smoking cessation
Cigarette smoke can acutely reduce airway cilliary function and
increase carbon monoxide levels.
* It may take weeks to months to find an objective improvement in
respiratory function after smoking cessation.
* The best evidence would suggest that at least two months is
required before smoking abstinence reduces the risk of pulmonary
complications .

Anesthetic technique :
The duration of anesthesia can impact the risk of respiratory
complications , significant reduction in mortality in those patients who
received neuraxial blockade or neuraxial blockade combined with
general anesthesia versus those who received general anesthesia
alone.
Pain control
Adequate postoperative pain control can reduce respiratory
complications in those incisions that are particularly painful (upper
abdominal and thorax). Segmental epidural blockade with local
anesthetics can increase tidal volume and vital capacity and improve
indices that reflect diaphragm activity after thoracic and upper
abdominal surgery.

 Postoperative lung expansion
A variety of techniques are available for postoperative lung
expansion. This includes incentive spirometry, assisted
cough, percussion and vibration, deep suctioning and
ambulation.

Definition of COPD
 Chronic obstructive pulmonary disease (COPD) is a spectrum of
diseases that includes emphysema, chronic bronchitis, and
asthmatic bronchitis. It is characterized by progressive increased
resistance to breathing. Airflow limitation may be caused by loss of
elastic recoil or obstruction of small or large (or both) conducting
airways.
 The increased resistance may have some degree of reversibility.
Cardinal symptoms are cough, dyspnea, and wheezing

Asthma
 Asthma is a common disorder, aﬀecting 5% to 7% of the population.
 Manifested by episodic attacks of dyspnea, cough, and wheezing
which is the result of bronchial smooth muscle constriction, edema,
and increased secretions
 The pathophysiology of asthma involves the local release of various
chemical mediators in the airway and, possibly, over activity of the
parasympathetic nervous system.
 Bronchoconstriction is the result of the subsequent release of
histamine; bradykinin; leukotrienes ; platelet-activating factor;
prostaglandins (PG) PGE2, PGF2, and PGD2; and neutrophil and
eosinophil chemotactic factors.

Patients with well-controlled asthma tend to have normal levels in
PFTs and arterial blood gas measurements and are not at risk for
major Postoperative complications . However, patients with
asthma with poor preoperative symptom control are at increased
risk of minor complications, such as bronchospasm.
Preoperative assessment & optimization :
1. History of illness, drugs, frequency of attacks.
2. Preoperative examination is the forced expiratory time (FET),
which is assessed by auscultation during expiration. FET values
greater than 6 seconds correlate with abnormal FEV1/FVC
ratios.
3. Patients should be advised to cease smoking at least 8 weeks
before surgery, and certain patients may benefit from a brief
course of corticosteroids.
4. Measurement of arterial blood gases is indicated if there is any
question about the adequacy of ventilation or oxygenation.
Anesthetic Preoperative Management

Asthmatic patients with active bronchospasm presenting for emergency
surgery should be treated aggressively whenever possible.
Supplemental oxygen, aerosolized B2 -agonists, and intravenous
glucocorticoids can dramatically improve lung function in a few hours.
In general, benzodiazepines are the most satisfactory agents for
premedication. Anticholinergic agents are not customarily given unless
very copious secretions are present or if ketamine is to be used for
induction of anesthesia.

The use of an H2- blocking agent (such as cimetidine, ranitidine, or
famotidine) is theoretically detrimental, since H2-receptor activation
normally produces bronchodilation.
Bronchodilators should be continued up to the time of surgery.
inhaled glucocorticoids, leukotriene blockers, mast-cell stabilizers,
theophyllines, and anticholinergics.

Intra operative Management Anesthetic
A goal of induction and maintenance of anesthesia is to suppress
airway reﬂexes to avoid bronchoconstriction in response to
mechanical stimulation of the airways.
a. Regional Anesthesia. The use of regional anesthesia when the
operative site is suitable for this may avoid instrumentation of the
airway and tracheal intubation.
b. General Anesthesia. Induction of anesthesia with propofol is
preferable to induction with thiopental, which is associated with a
higher incidence of wheezing. Ketamine may produce smooth
muscle relaxation and contribute to decreased airway resistance.

i. Intravenous or intratracheal injection of lidocaine 1 to 1.5 mg/kg
1 to 3 minutes before tracheal intubation can be helpful. Opioids
may suppress the cough reﬂex and deepen anesthesia. It may
be preferable to use short acting opioids that have limited risk of
causing postoperative respiratory depression, such as
remifentanil (continuous infusion of 0.05 to 0.1 mcg/kg/min).
ii. LMA insertion is less likely than endotracheal intubation to result in
bronchoconstriction and may be a better method of airway
management.
iii. Drugs with limited ability to evoke the release of histamine should
be selected.
Although all opioids have some histamine-releasing eﬀects, fentanyl
and analogous agents have been used safely in asthma patients.

iv. Antagonism of neuromuscular blockade with anticholinesterase
drugs could precipitate bronchospasm secondary to stimulation of
postganglionic cholinergic receptors in airway smooth muscle.
Bronchospasm does not predictably occur after administration of
anticholinesterase drugs, probably because of the protective
bronchodilating eﬀects provided by the simultaneous administration
of anticholinergic drugs.

v. During mechanical ventilation in asthmatic patients, a slow
inspiratory ﬂow rate provides optimal distribution of ventilation
relative to perfusion. Sufficient time for exhalation is necessary
to prevent air trapping. Humidification and warming of inspired
gases may be especially helpful.
vi. Maintenance of adequate hydration ensures less viscous
secretions in the airway.

vii. If possible, extubation should be performed while anesthesia
is still sufficient to suppress hyper reactive airway reﬂexes.
Suppressing airway reﬂexes and the risk of bronchospasm by
administration of intravenous lidocaine or pretreatment with
inhaled bronchodilators
should be considered.

Airﬂow obstruction during expiration is apparent on
capnography as a delayed rise of the end-tidal CO2
value.

Chronic Bronchitis
Chronic bronchitis is defined by the presence of a productive cough
on most days of 3 consecutive months for at least 2 consecutive
years.
Secretions from hypertrophied bronchial mucous glands and
mucosal edema from inflammation of the airways produce airflow
obstruction.
Intrapulmonary shunting is prominent, and hypoxemia is common.
In patients with COPD, chronic hypoxemia leads to erythrocytosis,
pulmonary hypertension, and eventually right ventricular failure (cor-
pulmonale); this combination of findings is often referred to as the
blue bloater syndrome.
In the course of disease progression, patients gradually develop
chronic CO2 retention; the normal ventilatory drive becomes less
sensitive to arterial CO2 tension and may be depressed by oxygen
administration

Emphysema
Pathological disorder characterized by irreversible enlargement of
the airways distal to terminal bronchioles and destruction of alveolar
septa.
Significant emphysema is nearly always related to cigarette smoking.
Less commonly, emphysema occurs at an early age and is
associated with a homozygous deficiency of alpha 1-antitrypsin.
Loss of the elastic recoil that normally supports small airways by
radial traction allows premature collapse during exhalation
Patients characteristically have increases in RV, FRC, TLC.

Large cystic areas, or bullae, develop in some patients.
Increased dead space is a prominent feature of emphysema.
Arterial oxygen tensions are usually normal or only slightly
reduced; CO2 tension is also typically normal.
When dyspneic, patients with emphysema often purse their lips to
delay closure of the small airways—which accounts for the term
pink puffers that is often used.

Treatment of COPD
Treatment for COPD is primarily supportive. The most important
intervention is cessation of smoking. Inhaled B2-adrenergic agonists,
glucocorticoids, and ipratropium are very useful.
Hypoxemia should be treated carefully with supplemental oxygen.
Oxygen therapy can dangerously elevate PaCO2 in patients with CO2
retention; elevating PaO2 above 60 mm Hg can precipitate respiratory
failure. When cor-pulmonale is present, diuretics are used to control
peripheral edema.

They should be questioned about recent changes in dyspnea,
sputum, and wheezing.
PFTs, chest radiographs, and arterial blood gas measurements
should be reviewed carefully.
In contrast to asthma, only limited improvement in respiratory
function may be seen after a short period of intensive preoperative
preparation.
preoperative interventions in patients with COPD aimed at
correcting hypoxemia, relieving bronchospasm, mobilizing and
reducing secretions, and treating infections may decrease the
incidence of postoperative pulmonary complications.

 Smoking should be discontinued for at least 6–8 weeks before
the operation to decrease secretions and to reduce pulmonary
complications.
cessation of smoking for as little as 24 h has theoretical beneficial
effects on the oxygen-carrying capacity of hemoglobin
Preoperative chest physiotherapy (chest percussion and postural
drainage) and antibiotics for patients with a change in sputum are
beneficial in reducing secretions.
 Bronchospasm should be treated with bronchodilators.
 Patients with moderate to severe disease may benefit from a
perioperative course of glucocorticoids.

Anesthetic Intra operative Management
Pre-oxygenation prior to induction of general anesthesia prevents
the rapid oxygen desaturation often seen in these patients.
The selection of anesthetic agents and general intraoperative
management are similar to those for asthmatic patients
ventilation should be controlled with small to moderate tidal
volumes and slow rates to avoid air trapping.
Humidified gases should be used if significant bronchospasm is
present and for long procedures (> 2 h).
Direct measurement of arterial oxygen tensions may be
necessary to detect more subtle changes in intrapulmonary
shunting.

Patients with pulmonary bullae are at high risk of developing
pneumothorax intraoperatively, particularly if ventilated with
positive pressure.
At the end of surgery, the timing of extubation should balance the
risk of bronchospasm with that of pulmonary insufficiency, but
evidence suggests that early extubation (in the operating room) is
beneficial.
Patients with an FEV1 below 50% are most likely to require a
period of postoperative ventilation, particularly following upper
abdominal and thoracic operations.

Bronchiectasis.
A chronic suppurative disease of the airways, bronchiectasis may
cause expiratory airﬂow obstruction similar to that seen with COPD.
1. Pathophysiology. Bacterial or mycobacterial infections are
presumed responsible for most cases of bronchiectasis.
2. Diagnosis. The history of a chronic cough productive of large
amounts of purulent sputum is highly suggestive of bronchiectasis.
Digital clubbing occurs in most patients with significant bronchiectasis.
Computed tomography (CT) provides excellent images of
bronchiectatic airways.

3. Treatment. Bronchiectasis is treated with antibiotics and
postural drainage. Massive hemoptysis (>200 mL over a 24-hour
period) may require surgical resection of the involved lung.
4. Management of Anesthesia. A double-lumen endobronchial
tube may be used to prevent spillage of purulent sputum into
normal areas of the lungs. Nasal intubation should be avoided
due to high rates of chronic sinusitis.

Restrictive Pulmonary Disease
 Restrictive pulmonary diseases are characterized by decreased lung
compliance.
 Lung volumes are typically reduced, with preservation of normal
expiratory flow rates.
 Both FEV1 and FVC are reduced, but the FEV1/FVC ratio is high or
normal.
 Restrictive pulmonary diseases include many acute and chronic
intrinsic pulmonary disorders as well as extrinsic (extra pulmonary)
disorders involving the pleura, chest wall, diaphragm, or
neuromuscular function.
 Reduced lung compliance increases the work of breathing, resulting
in a characteristic rapid but shallow breathing pattern.

Acute Intrinsic Pulmonary Disorders
 Acute intrinsic pulmonary disorders include pulmonary edema
(including the acute respiratory distress syndrome [ARDS]),
infectious pneumonia, and aspiration pneumonitis.
 Reduced lung compliance in these disorders is primarily due to
an increase in extravascular lung water, from either an increase
in pulmonary capillary pressure or an increase in pulmonary
capillary permeability
 Increased pressure occurs with left ventricular failure, whereas
fluid overload and increased permeability are present with
ARDS.

 In preparation for emergency procedures, oxygenation and
ventilation should be optimized preoperatively to the greatest extent
possible.
 Fluid overload should be treated with diuretics; heart failure may also
require vasodilators and inotrops.
 Persistent hypoxemia may require positive-pressure ventilation and
positive end-expiratory pressure (PEEP).

High inspired oxygen concentrations and PEEP may be required.
The decreased lung compliance results in high peak inspiratory
pressures during positive-pressure ventilation and increases the risk
of barotrauma and volutrauma.
Tidal volumes for these patients should be reduced to 4–7 mL/kg,
with a compensatory increase in the ventilatory rate (14–18
breaths/min), even if the result is an increase in end-tidal CO2..
Airway pressure should generally not exceed 30 cm H2O.

Chronic Intrinsic Pulmonary Disorders
Also often referred to as interstitial lung diseases.Characterized by
an insidious onset, chronic inflammation of alveolar walls and
progressive pulmonary fibrosis.
 Causes include : hypersensitivity pneumonitis from occupational
and environmental pollutants, drug toxicity (bleomycin and
nitrofurantoin), radiation pneumonitis, idiopathic pulmonary fibrosis,
autoimmune diseases, and sarcoidosis.
 Chronic pulmonary aspiration, oxygen toxicity, and severe ARDS
can also produce chronic fibrosis.

Patients typically present with dyspnea on exertion and sometimes
a nonproductive cough.
Symptoms of corpulmonale are present only with advanced
disease.
Physical examination may reveal fine (dry) crackles over the lung
bases and, in late stages, evidence of right ventricular failure.
The chest radiograph show "ground-glass" appearance and
"honeycomb" appearance.
Arterial blood gases usually show mild hypoxemia with
normocarbia.
PFTs are typical of a restrictive ventilatory defect

A history of dyspnea on exertion (or at rest) should be evaluated
further with PFTs and arterial blood gas analysis.
A vital capacity less than 15 mL/kg is indicative of severe
dysfunction (normal is > 70 mL/kg).
A chest radiograph is helpful in assessing disease severity.

The reduction in FRC (and oxygen stores) predisposes these patients to
rapid hypoxemia following induction of anesthesia; their uptake of
inhalation anesthetics may also be accelerated.
 Because these patients may be more susceptible to oxygen-induced
toxicity, particularly patients who have received bleomycin, the inspired
fractional concentration of oxygen should be kept to the minimum
concentration compatible with acceptable oxygenation (SpO2 of > 88–
92%).
 High peak inspiratory pressures during mechanical ventilation increase
the risk of pneumothorax and should prompt smaller than normal tidal
volumes with a faster rate.

Extrinsic Restrictive Pulmonary Disorders
 Extrinsic restrictive pulmonary disorders alter gas exchange by
interfering with normal lung expansion.
 They include pleural effusions, pneumothorax, mediastinal
masses, kyphoscoliosis, pectus excavatum, neuromuscular
disorders, and increased intraabdominal pressure from ascites,
pregnancy, or bleeding.
 Marked obesity also produces a restrictive ventilatory defect .
 Anesthetic considerations are similar to those discussed for
intrinsic restrictive disorders.

Pulmonary Embolism
 Pulmonary embolism results from the entry of blood clots, fat,
tumor cells, air, amniotic fluid, or foreign material into the venous
system. Venous stasis or hypercoagulability is often contributory
in such cases.
 Pulmonary embolism can also occur intraoperatively in normal
individuals undergoing certain procedures.

 The best treatment for pulmonary embolism is prevention.
 Heparin (unfractionated heparin 5000 U subcutaneously every 12
h begun preoperatively or immediately postoperatively in high-risk
patients), oral anticoagulation (warfarin), aspirin, or dextran
therapy together with early ambulation can decrease the incidence
of postoperative emboli.
 The use of high elastic stockings and pneumatic compression of
the legs may also decrease the incidence of venous thrombosis.
 Systemic anticoagulation prevents the formation of new blood clots
or the extension of existing clots. Heparin therapy is begun with
the goal of achieving an activated partial thromboplastin time of
1.5–2.4 times normal. Low-molecular-weight heparin (LMWH) is as
effective and is given subcutaneously at a fixed dose (based on
body weight) without laboratory monitoring.

 LMWH is more expensive than unfractionated heparin but is
more cost-effective. In high-risk patients, LMWH is started
either 12 h before surgery, 12–24 h after surgery, or at 50%
the usual dose 4–6 h after surgery. All patients should start
warfarin therapy concurrent with starting heparin therapy, and
the two should overlap for 4–5 days. The international
normalized ratio should be within the therapeutic range on
two consecutive measurements at least 24 h apart before the
heparin is stopped. Warfarin should be continued for 3–12
months.

 Patients with acute pulmonary embolism may present in the operating
room for placement of a caval filter or, rarely, for pulmonary
embolectomy.
 If the acute episode is more than 1 year old, the risk of temporarily
stopping anticoagulant therapy is probably small.

 Vena cava filters are usually placed percutaneously under local
anesthesia with sedation.
 Decreased venous return during placement of the device can
precipitate hypotension.
 Patients presenting for pulmonary embolectomy are critically ill.
They are usually already intubated but tolerate positive-pressure
ventilation poorly. Inotropic support is necessary until the clot is
removed.
 They also tolerate all anesthetic agents very poorly. Small doses of
an opioid, etomidate, or ketamine may be used, but the latter can
theoretically increase pulmonary artery pressures. Cardiopulmonary
bypass is required.

Intra operative Pulmonary Embolism
 Significant pulmonary embolism is a rare occurrence during
anesthesia.
 Air emboli are common but are often overlooked unless large
amounts are entrained.
 Fat embolism can occur during orthopedic procedures; amniotic fluid
embolism is a rare, unpredictable, and often fatal, complication of
obstetrical delivery .
 Thromboembolism may occur intraoperatively during prolonged
procedures.
 The clot may have been present prior to surgery or may form
intraoperatively; surgical manipulations or a change in the patient's
position may then dislodge the venous thrombus. Manipulation of
tumors with intravascular extension can similarly produce pulmonary
embolism.

Intra operative management of PE
1. Intraoperative pulmonary embolism usually presents as:
2. unexplained sudden hypotension, hypoxemia, or bronchospasm.
3. A decrease in end-tidal CO2 concentration.
4. Elevated central venous and pulmonary arterial pressures.
5. Transesophageal echocardiogram may be helpful.
Management:
 If air is identified in the right atrium, or if it is suspected,
emergent central vein cannulation and aspiration of the air may
be lifesaving.
 For all other emboli, treatment is supportive, with intravenous fluids
and inotropes.
 Placement of a vena cava filter should be considered
postoperatively.

Postoperative lung expansion
A variety of techniques are available for postoperative lung
expansion. This includes
1. Incentive spirometry.
2. Assisted cough.
3. Percussion and vibration.
4. Deep suctioning.
5. Early Ambulation.
The use of postoperative incentive spirometry has been shown
to reduce postoperative respiratory complications

Anesthesia in patient with respiratory disease

Anesthesia in patient with respiratory disease

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